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52. Long noncoding RNA LINC00305 promotes inflammation by activating the AHRR-NF-κB pathway in human monocytes

Author

Zhang, Dan-Dan, primary, Wang, Wen-Tian, additional, Xiong, Jian, additional, Xie, Xue-Min, additional, Cui, Shen-Shen, additional, Zhao, Zhi-Guo, additional, Li, Mulin Jun, additional, Zhang, Zhu-Qin, additional, Hao, De-Long, additional, Zhao, Xiang, additional, Li, Yong-Jun, additional, Wang, Junwen, additional, Chen, Hou-Zao, additional, Lv, Xiang, additional, and Liu, De-Pei, additional

Published
2017
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53. Diurnal oscillations of endogenous H2O2sustained by p66Shcregulate circadian clocks

Author

Pei, Jian-Fei, Li, Xun-Kai, Li, Wen-Qi, Gao, Qian, Zhang, Yang, Wang, Xiao-Man, Fu, Jia-Qi, Cui, Shen-Shen, Qu, Jia-Hua, Zhao, Xiang, Hao, De-Long, Ju, Dapeng, Liu, Na, Carroll, Kate S., Yang, Jing, Zhang, Eric Erquan, Cao, Ji-Min, Chen, Hou-Zao, and Liu, De-Pei

Abstract

Redox balance, an essential feature of healthy physiological steady states, is regulated by circadian clocks, but whether or how endogenous redox signalling conversely regulates clockworks in mammals remains unknown. Here, we report circadian rhythms in the levels of endogenous H2O2in mammalian cells and mouse livers. Using an unbiased method to screen for H2O2-sensitive transcription factors, we discovered that rhythmic redox control of CLOCK directly by endogenous H2O2oscillations is required for proper intracellular clock function. Importantly, perturbations in the rhythm of H2O2levels induced by the loss of p66Shc, which oscillates rhythmically in the liver and suprachiasmatic nucleus (SCN) of mice, disturb the rhythmic redox control of CLOCK function, reprogram hepatic transcriptome oscillations, lengthen the circadian period in mice and modulate light-induced clock resetting. Our findings suggest that redox signalling rhythms are intrinsically coupled to the circadian system through reversible oxidative modification of CLOCK and constitute essential mechanistic timekeeping components in mammals.

Published
2019
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55. Age-Associated Sirtuin 1 Reduction in Vascular Smooth Muscle Links Vascular Senescence and Inflammation to Abdominal Aortic Aneurysm

Author

Chen, Hou-Zao, primary, Wang, Fang, additional, Gao, Peng, additional, Pei, Jian-Fei, additional, Liu, Yue, additional, Xu, Ting-Ting, additional, Tang, Xiaoqiang, additional, Fu, Wen-Yan, additional, Lu, Jie, additional, Yan, Yun-Fei, additional, Wang, Xiao-Man, additional, Han, Lei, additional, Zhang, Zhu-Qin, additional, Zhang, Ran, additional, Zou, Ming-Hui, additional, and Liu, De-Pei, additional

Published
2016
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63. Correction: Corrigendum: Interferon regulatory factor 9 is critical for neointima formation following vascular injury

Author

Zhang, Shu-Min, primary, Zhu, Li-Hua, additional, Chen, Hou-Zao, additional, Zhang, Ran, additional, Zhang, Peng, additional, Jiang, Ding-Sheng, additional, Gao, Lu, additional, Tian, Song, additional, Wang, Lang, additional, Zhang, Yan, additional, Wang, Pi-Xiao, additional, Zhang, Xiao-Fei, additional, Zhang, Xiao-Dong, additional, Liu, De-Pei, additional, and Li, Hongliang, additional

Published
2015
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69. Interferon regulatory factor 9 is critical for neointima formation following vascular injury

Author

Zhang, Shu-Min, primary, Zhu, Li-Hua, additional, Chen, Hou-Zao, additional, Zhang, Ran, additional, Zhang, Peng, additional, Jiang, Ding-Sheng, additional, Gao, Lu, additional, Tian, Song, additional, Wang, Lang, additional, Zhang, Yan, additional, Wang, Pi-Xiao, additional, Zhang, Xiao-Fei, additional, Zhang, Xiao-Dong, additional, Liu, De-Pei, additional, and Li, Hongliang, additional

Published
2014
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72. The Involvement of NFAT Transcriptional Activity Suppression in SIRT1-Mediated Inhibition of COX-2 Expression Induced by PMA/Ionomycin

Author

Jia, Yu-Yan, primary, Lu, Jie, additional, Huang, Yue, additional, Liu, Guang, additional, Gao, Peng, additional, Wan, Yan-Zhen, additional, Zhang, Ran, additional, Zhang, Zhu-Qin, additional, Yang, Rui-Feng, additional, Tang, Xiaoqiang, additional, Xu, Jing, additional, Wang, Xu, additional, Chen, Hou-Zao, additional, and Liu, De-Pei, additional

Published
2014
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76. Mouse macrophage specific knockout of SIRT1influences macrophage polarization and promotes angiotensin II-induced abdominal aortic aneurysm formation

Author

Zhang, Zhuqin, Xu, Jing, Liu, Yue, Wang, Tingting, Pei, Jianfei, Cheng, Liqin, Hao, Delong, Zhao, Xiang, Chen, Hou-Zao, and Liu, De-Pei

Abstract

Abdominal aortic aneurysm (AAA) is a vascular degenerative disease. Macrophage polarization and the balance between classically activated macrophages (M1) and alternatively activated macrophages (M2) are crucial for AAA pathogenesis. The present study aims to investigate the roles of macrophage SIRT1 in AAA formation and macrophage polarization. We found that in mouse peritoneal macrophages, SIRT1 expression was decreased after M1 stimulation, but was enhanced after M2 stimulation. Results from SIRT1flox/floxmice and macrophage specific SIRT1knockout mice with treatment of angiotensin II (Ang II) for 4 weeks showed that macrophage specific deficiency of SIRT1 increased the incidence of AAA and exacerbated the severity, including more severe aneurysm types, enlarged diameter of the aneurysm and increased degradation of elastin. In mouse aortas, SIRT1 deficiency increased the pro-inflammatory M1 molecule inducible nitric oxide synthase (iNOS), and decreased M2 molecules such as arginase 1 (Arg1) and mannose receptor (MR). Furthermore, in peritoneal macrophages, SIRT1 deficiency increased the expression of M1 inflammatory molecules, but decreased the expression of M2 molecules. Overexpression of SIRT1 had the opposite effects. Thus, macrophage specific knockout of SIRT1influences macrophage polarization and accelerates Ang II-induced AAA formation.

Published
2018
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81. Repression of P66Shc Expression by SIRT1 Contributes to the Prevention of Hyperglycemia-Induced Endothelial Dysfunction

Author

Zhou, Shuang, primary, Chen, Hou-Zao, additional, Wan, Yan-zhen, additional, Zhang, Qing-Jun, additional, Wei, Yu-Sheng, additional, Huang, Shuai, additional, Liu, Jin-Jing, additional, Lu, Yun-Biao, additional, Zhang, Zhu-Qin, additional, Yang, Rui-Feng, additional, Zhang, Ran, additional, Cai, Hua, additional, Liu, De-Pei, additional, and Liang, Chih-Chuan, additional

Published
2011
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82. Positive regulation of hepatic miR-122 expression by HNF4α

Author

Li, Zhen-Ya, primary, Xi, Yang, additional, Zhu, Wen-Nan, additional, Zeng, Chao, additional, Zhang, Zhu-Qin, additional, Guo, Zhi-Chen, additional, Hao, De-Long, additional, Liu, Guang, additional, Feng, Lei, additional, Chen, Hou-Zao, additional, Chen, Feng, additional, Lv, Xiang, additional, Liu, De-Pei, additional, and Liang, Chih-Chuan, additional

Published
2011
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83. SIRT1 Acts as a Modulator of Neointima Formation Following Vascular Injury in Mice

Author

Li, Li, primary, Zhang, Hui-Na, additional, Chen, Hou-Zao, additional, Gao, Peng, additional, Zhu, Li-Hua, additional, Li, Hong-Liang, additional, Lv, Xiang, additional, Zhang, Qing-Jun, additional, Zhang, Ran, additional, Wang, Zhao, additional, She, Zhi-Gang, additional, Wei, Yu-Sheng, additional, Du, Guan-Hua, additional, Liu, De-Pei, additional, and Liang, Chih-Chuan, additional

Published
2011
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87. Human Paraoxonase Gene Cluster Transgenic Overexpression Represses Atherogenesis and Promotes Atherosclerotic Plaque Stability in ApoE-Null Mice

Author

She, Zhi-Gang, primary, Zheng, Wei, additional, Wei, Yu-Sheng, additional, Chen, Hou-Zao, additional, Wang, Ai-Bing, additional, Li, Hong-Liang, additional, Liu, Guang, additional, Zhang, Ran, additional, Liu, Jin-Jing, additional, Stallcup, William B., additional, Zhou, Zhongjun, additional, Liu, De-Pei, additional, and Liang, Chih-Chuan, additional

Published
2009
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88. A20 inhibits oxidized low‐density lipoprotein‐induced apoptosis through negative Fas/Fas ligand‐dependent activation of caspase‐8 and mitochondrial pathways in murine RAW264.7 macrophages

Author

Li, Hong‐Liang, primary, Wang, Ai‐Bing, additional, Zhang, Ran, additional, Wei, Yu‐Sheng, additional, Chen, Hou‐Zao, additional, She, Zhi‐Gang, additional, Huang, Yue, additional, Liu, De‐Pei, additional, and Liang, Chih‐Chuan, additional

Published
2006
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90. Abstract 236.

Author

Liu, De-Pei, Zhang, Zhu-Qin, Ren, Si-Cong, Li, Zuo-Zhi, Tan, Ying, Tang, Xiao-Qiang, Hao, De-Long, Guo, Zhi-Chen, Zhao, Xiang, and Chen, Hou-Zao

Published
2014

92. The histone trimethyllysine demethylase JMJD2A promotes cardiac hypertrophy in response to hypertrophic stimuli in mice.

Author

Qing-Jun Zhang, Hou-Zao Chen, Lin Wang, De-Pei Liu, Hill, Joseph A., Zhi-Ping Liu, Zhang, Qing-Jun, Chen, Hou-Zao, Wang, Lin, Liu, De-Pei, and Liu, Zhi-Ping

Subjects
*CARDIAC hypertrophy, *HISTONES, *METHYLATION, *CHROMATIN, *PHENOTYPES, *TRANSCRIPTION factors, *LABORATORY mice, *CELL metabolism, *PROTEIN metabolism, *NUCLEAR proteins, *ANIMAL experimentation, *AORTIC diseases, *CELL culture, *CELLS, *COMPARATIVE studies, *DNA, *DOCUMENTATION, *GENES, *HEART failure, *RESEARCH methodology, *MEDICAL cooperation, *MICE, *MUSCLE proteins, *NUCLEOTIDES, *OXIDOREDUCTASES, *PROTEINS, *RATS, *RESEARCH, *RNA, *EVALUATION research, *VENTRICULAR remodeling, *STENOSIS, *SIGNAL peptides, *LEFT ventricular hypertrophy, *DISEASE complications, *PHYSIOLOGY
Abstract

Cardiac hypertrophy and failure are accompanied by a reprogramming of gene expression that involves transcription factors and chromatin remodeling enzymes. Little is known about the roles of histone methylation and demethylation in this process. To understand the role of JMJD2A, a histone trimethyl demethylase, in cardiac hypertrophy, we generated mouse lines with heart-specific Jmjd2a deletion (hKO) and overexpression (Jmjd2a-Tg). Jmjd2a hKO and Jmjd2a-Tg mice had no overt baseline phenotype, but did demonstrate altered responses to cardiac stresses. While inactivation of Jmjd2a resulted in an attenuated hypertrophic response to transverse aortic constriction-induced (TAC-induced) pressure overload, Jmjd2a-Tg mice displayed exacerbated cardiac hypertrophy. We identified four-and-a-half LIM domains 1 (FHL1), a key component of the mechanotransducer machinery in the heart, as a direct target of JMJD2A. JMJD2A bound to the FHL1 promoter in response to TAC, upregulated FHL1 expression, and downregulated H3K9 trimethylation. Upregulation of FHL1 by JMJD2A was mediated through SRF and myocardin and required its demethylase activity. The expression of JMJD2A was upregulated in human hypertrophic cardiomyopathy patients. Our studies reveal that JMJD2A promotes cardiac hypertrophy under pathological conditions and suggest what we believe to be a novel mechanism for JMJD2A in reprogramming of gene expression involved in cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Published
2011
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93. [Study of senescence protein p66 Shc on myocardial tissue repair in adult mice].

Author

Zhang Y, Huang CZ, Chen HZ, Nie Y, and Hu MQ

Subjects
Animals, Mice, Body Weight, Cicatrix metabolism, Mice, Knockout, Shc Signaling Adaptor Proteins metabolism, Src Homology 2 Domain-Containing, Transforming Protein 1 genetics, Src Homology 2 Domain-Containing, Transforming Protein 1 metabolism, Myocardial Infarction genetics, Oxidative Stress
Abstract

Our previous study has shown that p66 Shc plays an important role in the process of myocardial regeneration in newborn mice, and p66 Shc deficiency leads to weakened myocardial regeneration in newborn mice. This study aims to explore the role of p66 Shc protein in myocardial injury repair after myocardial infarction in adult mice, in order to provide a new target for the treatment of myocardial injury after myocardial infarction. Mouse myocardial infarction models of adult wild-type (WT) and p66 Shc knockout (KO) were constructed by anterior descending branch ligation. The survival rate and heart-to-body weight ratio of two models were compared and analyzed. Masson's staining was used to identify scar area of injured myocardial tissue, and myocyte area was determined by wheat germ agglutinin (WGA) staining. TUNEL staining was used to detect the cardiomyocyte apoptosis. The protein expression of brain natriuretic peptide (BNP), a common marker of myocardial hypertrophy, was detected by Western blotting. The results showed that there was no significant difference in survival rate, myocardial scar area, myocyte apoptosis, and heart weight to body weight ratio between the WT and p66 Shc KO mice after myocardial infarction surgery. Whereas the protein expression level of BNP in the p66 Shc KO mice was significantly down-regulated compared with that in the WT mice. These results suggest that, unlike in neonatal mice, the deletion of p66 Shc has no significant effect on myocardial injury repair after myocardial infarction in adult mice.

Published
2023

94. Vascular Transcriptome Profiling Reveals Aging-Related Genes in Angiotensin Ⅱ-Induced Hypertensive Mouse Aortas.

Author

Lv SJ, Ding YN, Pei XY, Zhao X, Hao L, Zhang ZQ, Chen HZ, and Liu P

Subjects
Angiotensin II, Animals, Aorta physiopathology, Blood Pressure genetics, Gene Ontology, Hypertension chemically induced, Male, Mice, Inbred C57BL, Reverse Transcriptase Polymerase Chain Reaction, Aging, Aorta metabolism, Gene Expression Profiling methods, Hypertension genetics
Abstract

Objective Angiotensin Ⅱ (Ang Ⅱ)-induced vascular damage is a major risk of hypertension. However, the underlying molecular mechanism of AngⅡ-induced vascular damage is still unclear. In this study, we explored the novel mechanism associated with Ang II-induced hypertension. Methods We treated 8- to 12-week-old C57BL/6J male mice with saline and Ang Ⅱ(0.72 mg/kg·d) for 28 days, respectively. Then the RNA of the media from the collected mice aortas was extracted for transcriptome sequencing. Principal component analysis was applied to show a clear separation of different samples and the distribution of differentially expressed genes was manifested by Volcano plot. Functional annotations including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway were performed to reveal the molecular mechanism of Ang Ⅱ-induced hypertension. Finally, the differentially expressed genes were validated by using quantitative real-time PCR. Results The result revealed that a total of 773 genes, including 599 up-regulated genes and 174 down-regulated genes, were differentially expressed in the aorta of Ang Ⅱ-induced hypertension mice model. Functional analysis of differentially expressed genes manifested that various cellular processes may be involved in the Ang Ⅱ-induced hypertension, including some pathways associated with hypertension such as extracellular matrix, inflammation and immune response. Interestingly, we also found that the differentially expressed genes were enriched in vascular aging pathway, and further validated that the expression levels of insulin-like growth factor 1 and adiponectin were significantly increased ( P <0.05). Conclusion We identify that vascular aging is involved in Ang Ⅱ-induced hypertension, and insulin-like growth factor 1 and adiponectin may be important candidate genes leading to vascular aging.

Published
2020
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95. SIRT4 accelerates Ang II-induced pathological cardiac hypertrophy by inhibiting manganese superoxide dismutase activity.

Author

Luo YX, Tang X, An XZ, Xie XM, Chen XF, Zhao X, Hao DL, Chen HZ, and Liu DP

Subjects
Angiotensin II pharmacology, Animals, Gene Knockdown Techniques, Male, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Heart enzymology, Myocytes, Cardiac enzymology, Oxidative Stress physiology, Reactive Oxygen Species antagonists & inhibitors, Vascular Remodeling physiology, Vasoconstrictor Agents pharmacology, Cardiomegaly enzymology, Mitochondrial Proteins physiology, Sirtuins physiology, Superoxide Dismutase antagonists & inhibitors
Abstract

Aims: Oxidative stress contributes to the development of cardiac hypertrophy and heart failure. One of the mitochondrial sirtuins, Sirt4, is highly expressed in the heart, but its function remains unknown. The aim of the present study was to investigate the role of Sirt4 in the pathogenesis of pathological cardiac hypertrophy and the molecular mechanism by which Sirt4 regulates mitochondrial oxidative stress., Methods and Results: Male C57BL/6 Sirt4 knockout mice, transgenic (Tg) mice exhibiting cardiac-specific overexpression of Sirt4 (Sirt4-Tg) and their respective controls were treated with angiotensin II (Ang II, 1.1 mg/kg/day). At 4 weeks, hypertrophic growth of cardiomyocytes, fibrosis and cardiac function were analysed. Sirt4 deficiency conferred resistance to Ang II infusion by significantly suppressing hypertrophic growth, and the deposition of fibrosis. In Sirt4-Tg mice, aggravated hypertrophy and reduced cardiac function were observed compared with non-Tg mice following Ang II treatment. Mechanistically, Sirt4 inhibited the binding of manganese superoxide dismutase (MnSOD) to Sirt3, another member of the mitochondrial sirtuins, and increased MnSOD acetylation levels to reduce its activity, resulting in elevated reactive oxygen species (ROS) accumulation upon Ang II stimulation. Furthermore, inhibition of ROS with manganese 5, 10, 15, 20-tetrakis-(4-benzoic acid) porphyrin, a mimetic of SOD, blocked the Sirt4-mediated aggravation of the hypertrophic response in Ang II-treated Sirt4-Tg mice., Conclusions: Sirt4 promotes hypertrophic growth, the generation of fibrosis and cardiac dysfunction by increasing ROS levels upon pathological stimulation. These findings reveal a role of Sirt4 in pathological cardiac hypertrophy, providing a new potential therapeutic strategy for this disease., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2016. For permissions please email: journals.permissions@oup.com.)

Published
2017
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96. A critical role for interferon regulatory factor 9 in cerebral ischemic stroke.

Author

Chen HZ, Guo S, Li ZZ, Lu Y, Jiang DS, Zhang R, Lei H, Gao L, Zhang X, Zhang Y, Wang L, Zhu LH, Xiang M, Zhou Y, Wan Q, Dong H, Liu DP, and Li H

Subjects
Acetylation, Animals, Cells, Cultured, Humans, Infarction, Middle Cerebral Artery pathology, Interferon-Stimulated Gene Factor 3, gamma Subunit genetics, Male, Mice, Mice, Inbred C57BL, Neurons pathology, Sirtuin 1 metabolism, Stroke pathology, Tumor Suppressor Protein p53 metabolism, Apoptosis, Infarction, Middle Cerebral Artery metabolism, Interferon-Stimulated Gene Factor 3, gamma Subunit metabolism, Neurons metabolism, Stroke metabolism
Abstract

The failure of past efforts to develop effective stroke treatments is at least partially because these treatments often interfered with essential physiological functions, even though they are targeted toward pathophysiological events, such as inflammation, excitotoxicity, and oxidative stress. Thus, the direct targeting of endogenous neuroprotective or destructive elements holds promise as a potential new approach to treating this devastating condition. Interferon regulatory factor 9 (IRF9), a transcription factor that regulates innate immune responses, has been implicated in neurological pathology. Here, we provide new evidence that IRF9 directly mediates neuronal death in male mice. In response to ischemia/reperfusion (I/R), IRF9 accumulated in neurons. IRF9 deficiency markedly mitigated both poststroke neuronal death and neurological deficits, whereas the neuron-specific overexpression of IRF9 sensitized neurons to death. The histone deacetylase Sirt1 was identified as a novel negative transcriptional target of IRF9 both in vivo and in vitro. IRF9 inhibits Sirt1 deacetylase activity, culminating in the acetylation and activation of p53-mediated cell death signaling. Importantly, both the genetic and pharmacological manipulation of Sirt1 effectively counteracted the pathophysiological effects of IRF9 on stroke outcome. These findings indicate that, rather than activating a delayed innate immune response, IRF9 directly activates neuronal death signaling pathways through the downregulation of Sirt1 deacetylase in response to acute I/R stress., (Copyright © 2014 the authors 0270-6474/14/3411897-16$15.00/0.)

Published
2014
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97. [Research progression of deacetylase (SIRT1)].

Author

Chen HZ, Zhang ZQ, Wei YS, and Liu DP

Subjects
Animals, Caloric Restriction, Humans, Longevity, Sirtuin 1 genetics, Substrate Specificity, Sirtuin 1 physiology
Abstract

The silent information regulator protein 2 (Sir2) and its homologues play an important role in the regulation of cellular physiological processes such as survival, apoptosis, and aging. SIRT1, the mammalian Sir 2 homologue, has been shown to deacetylate a wide range of non-histone substrates and histone substrates. It has been constantly reported that SIRT1 may be associated with the occurrence of metabolic syndrome, genomic homeostasis, tumors, and neurodegenerative diseases. Calorie restriction may mitigate many major diseases in rodent models by SIRT1-mediated deacetylase activity and prolong the life expectancies in these animals. Therefore, SIRT1 may be emphasized as a new therapy target for many different diseases.

Published
2007

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